Ischemia-modified albumin (IMA) has been proposed as a biological marker of myocardial ischemia (1, 2 ). Exposure to ischemic myocardium modifies circulating albumin at its NH 2 terminus by different mechanisms, and this modification is the basis of IMA measurement by the albumin cobalt binding (ACB) test (3 ). The tissue-specific nature of the mechanism by which ischemia modifies albumin remains undetermined. Together with a nondiagnostic electrocardiogram and negative troponin values, IMA concentrations within the reference interval have high negative predictive value of myocardial ischemia in patients with suspected acute coronary syndromes (1, 2 ). However, IMA cardiospecificity has not been validated and needs an evidence base before routine clinical use. A recent report showed significant IMA increases 24 -48 h after a marathon race, with exercise-promoted gastrointestinal and/or delayed skeletal muscle ischemia being evoked as possible causes of such increases (4 ). However, because IMA has shown rapid kinetics of increase (in minutes) and return to baseline no longer than 12 h after angioplastic procedures (5 ), long-duration skeletal muscle ischemia (i.e., occurring during marathons) does not appear to be the most appropriate model to investigate the effect of such ischemia on IMA values or the kinetics of IMA occurring during acute coronary syndromes. The aim of this work was to analyze the possible contribution of skeletal muscle ischemia to IMA by investigating its short-term kinetics in an isolated skeletal-muscle ischemia model. Because lactate and ammonia concentrations increase sharply after a forearm ischemia test, their possible influence in the ACB assay was studied.Ten healthy volunteers (4 men and 6 women) from our laboratory staff (age range, 48 -61 years; median, 53 years) with no personal or family history of cardiovascular disease and no known cardiovascular risk factors after a medical examination underwent a forearm ischemia test (6 ). Briefly, after an overnight fast (10 -12 h) and 30 min of previous rest, a preexercise (0 min) blood sample was drawn, and blood systolic pressure was recorded twice within a 5-min interval. Thereafter, forearm ischemia was produced by inflating the blood pressure cuff up to 20 -30 mmHg higher than the maximum systolic pressure registered. Under these ischemic conditions, a hand-grip exercise at maximum possible strength was performed for 1 min. Thereafter, the cuff was removed, and serial blood samples were drawn at 1, 3, 5, 10, 15, and 30 min. Serum for IMA, creatine kinase, and potassium; EDTA plasma for ammonia; and fluoride plasma for lactate and glucose were collected at each time point into Vacutainer ® Tubes (Becton Dickinson). To establish reference values, IMA was tested in a group of 86 fasting (10 -12 h), ambulatory (median age, 57 years; 38 women) sedentary individuals who underwent blood sampling after health examinations or before minor surgical procedures. Individuals with cardiovascular risk factors or past or present signs or symptoms o...

Oral d,l-sotalol is effective and safe in patients with VT/VF. However, sudden cardiac death develops in a significant proportion of patients, and programmed stimulation seems to be of limited value for its prediction.

Animplantable cardioverter-defibrillator tachycardia detection algorithm with a stability criterion of 50 to 60 ms and 12 to 14 RR intervals is able to detect over 90% of monomorphic irregular VTs. Nevertheless, significant VT detection delays may arise, and inappropriate detection of AF cannot be totally prevented.

The role of programmed ventricular stimulation (PVS) in patients at high risk of sudden death related to idiopathic dilated cardiomyopathy (DCM) is still controversial. The possible reason is that most study series have been too small or that only a few patients had documented sustained ventricular tachyarrhythmias. This study therefore, looked at PVS performed in 102 patients with DCM and documented sustained ventricular tachycardia (VT; n = 63) or ventricular fibrillation (VF; n = 39). Sustained VT was induced in 27 of 63 patients (43%) with documented sustained VT and in 14 of 39 patients (36%) with documented VF (ns). VF was induced in nine patients (14%) with a history of sustained VT and in seven (18%) with a history of VF (ns). At a mean follow-up of 32 +/- 15 months, sudden death occurred in 14 (14%) patients, a rate similar in both patients with documented VT and VF (ns). Incidence of sudden death at 36 months was 6% in patients with inducible sustained VT/VF compared to 29% in patients without inducible VT/VF (P < 0.05). A favourable drug regimen (response to drug and no intolerable side effects) was obtained by serial drug testing in 25 of all 102 patients (25%). A cardioverter defibrillator (ICD) was implanted in 32 patients, in 63% of whom discharges were observed during 18 +/- 11 months of follow-up; only one patient (3%) died suddenly. Thus, in patients with DCM, there was no relationship between documented and inducible ventricular tachyarrhythmias, and initiation of sustained VT or VF had little prognostic value for the prediction of subsequent sudden death. Wherever antiarrhythmic drug therapy was of limited value, implantation of an ICD may improve the prognosis of these high risk patients.

After initially successful ablation, the recurrence rates of accessory pathway conduction at 1, 3, and 6 months were 5.9%, 7.4%, and 11.3%, respectively. Late electrophysiologic testing had little prognostic value in asymptomatic patients following successful ablation. Application of "safety pulses" did not prevent recurrence. Late block of accessory pathway conduction did not predict long-term efficacy.